New Insights into the Role of Vitamin D in Athletes: Soccer Players Offer Ideal Study Subjects - Vitamin D (25-OHD) Predicts Performance, Training Season Predicts Vitamin D

Not the ideal soccer weather. If you put faith in the authors' interpretation of the results, soccer is a game that must be played in the sun. Why? Well, to maximize the vitamin D production ;-)

It has been a while since I have seen a study on vitamin D that provides new-worthy results beyond the obvious "vitamin D supplements are useless in men and women with normal 25-OHD levels". The study I am about to talk about today was conducted by researchers from the University of Crete. The subjects were sixty seven Caucasian professional male soccer players, members of two Greek Super League Teams (n = 45) and one Football League Team (n = 22). The goal was to (a) examine the potential relationship between vitamin D levels and muscle strength, maximal oxygen consumption (VO2max), 10 and, 20 meters sprint performance in two different occasions, prior to the beginning and at the end of the off-season soccer period; and (b) to examine the vitamin D response to the reduced exercise training during the six-week off-season transition period.

The authors speculated that in both experimental sessions vitamin D levels would correlate with soccer players’ jumping, sprinting, and aerobic capacity, and that the off-season transition period, of reduced training stress, would favorably affect vitamin D concentration.

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As we are about to see a few lines below, this is exactly what Nikolaos E. Koundourakis and his colleagues found in what is "to the best of [the researchers] knowledge" the first study to examine the relationship "between vitamin D levels and muscle strength, VO2max and speed in professional soccer players, and/or the effects off-season detraining soccer period on its levels in any kind of athletic population." (Koundourakis. 2014)

Table 1: Correlations (correlation coefficients and p-values) between Vitamin D levels and exercise performance parameters; pre = acute pre-season training vs. post = after six-week off-season transition period (Koundourakis. 2014)

As you can see in Table 1, there was a significant correlation between the strength measures squat jump (SJ) and countermovement jump (CMJ), as well as with VO2max and the 10m and 20m sprint times. There was jet also a significant increase in vitamin D from pre to post season, i.e from 34.41 to 47.21ng/ml (37%) of which Koundourakis et al. write the following:

Suggested Read: Leucine, Insulin & Vitamin D: A Hypertrophy Boosting Triplet That Does Not Make It From the Dish to the Gym? | read more

"In our study the six-week transition period had a boosting effect on vitamin D levels. Indeed, at the first experimental period,although none of our participants was vitamin D deficient (<20 ng/ml) or severe deficient (<10 ng/ml), 55,22% of our players had insufficient vitamin D levels (<30 ng/ml), whereas at the second one only 4,47% were found to be below 30 ng/ml. [...] The most plausible explanation for the elevation of vitamin D levels at the second experimental session could be the consequence of an increased exposure to UVB during the off-season period.

Indeed, this transition period in Greek Superleague takes place during June and at the beginning of July at a favorable latitude (35,9°N). During this period UVB reaches its peak, resulting in increased vitamin D production." (Koundourakis. 2014)

These observations highlight the importance of adequate sun exposure and raise the question, whether it wouldn't be prudent to supplement with 2.000IU of vitamin D per day during the winter months to avoid the reduction in vitamin D levels in the first place.

Tanning beds are neither suitable to get your vitamin D levels up (many don't even radiate UV-B light / it's also blocked by glass), tanning on a sunbed is also not safer than doing the same in the sun | more

There is a different explanation: Next to the sun-exposure hypothesis, there is another possible reason for the increase in vitamin D, which would be related to the (albeit beneficial) stress the soccer players are exposed to during each and every of their training sessions. If vitamin D was the negative acute phase reactant, Waldron et al. say it was (2013), it would be logical that the levels increase in the absence of acute stressors.

Needless to say that the latter wouldn't make getting enough UV exposure obsolete - an exposure you better get in the real sun than on one of the allegedly less problematic tanning beds, which lack the vitamin D production kickstarting UV-B radiation.

References:

• Koundourakis, Nikolaos E., et al. "Vitamin D and Exercise Performance in Professional Soccer Players." PLOS ONE 9.7 (2014): e101659.
• Waldron, Jenna Louise, et al. "Vitamin D: a negative acute phase reactant." Journal of clinical pathology (2013): jclinpath-2012.

Based on the Latest Evidence, Who Would Benefit From Even more Vitamin D? Plus: How Much Vitamin D Do I Need To Achieve Optimal Levels & Keep Them Steady?

Injecting large doses of vitamin D is unnecessary to get into the normal range and everything way above 35ng/ml could be doing more harm than good.

It's not as hot as it's use to be, but the token "vitamin" will still produce mostly studies dealing with "vitamin D", when you type it into the search field of PubMed or any other medical database search. Against that background, it's almost pathetic that "information regarding the associations between vitamin D and inflammatory markers in the general population is sparse" (Hannemann. 2014) - we know the non-classical effects of vitamin D on the innate and adaptive immunity for 30 years and still, at least for Germany only few studies assessed the relation between vitamin D and chronic inflammation in a way that would allow us to answer the question I posed in the title of today's SuppVersity article.

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In their latest paper in the peer-revied scientific journal Metabolism, Liesa Mellenthin, Henri Wallaschofski, Anne Grotevendt, Henry Völzke, Matthias Nauck, and Anke Hannemann from the University of Greifwald present the corresponding data. Data from 2723 men and women aged 25-88
years who were part of the first follow-up of the Study of Health in Pomerania.

Figure 1: Vitamin D status of the 2723 men and women in the Study of Health in Pomerania (Mellenthin. 2014)

As you can see in Figure 1 the number of Germans with low vitamin D levels is significant. The number of subjects in the target range of >30ng/ml 25OHD, on the other hand, was comparatively low.

The selected few are at a disadvantage

Interestingly, those "selected few" who are "in the zone", were  not the ones with the lowest levels of hs-CRP, the contemporary standard marker of whole body inflammation.

Vitamin D status	Hs-CRP	Fibrinogen	White blood cell count
			Smoker	Non-smoker
Deficiency (n = 322)	1.40 (0.88-2.22)	Reference	Reference	Reference
Insufficiency (n = 1301)	1.27 (0.91-1.78)	0.75 (0.51-1.09)	0.92 (0.52-1.61)	0.69 (0.39-1.22)
Sufficiency (n = 744)	Reference	0.69 (0.44-1.06)	0.59 (0.29-1.17)	0.79 (0.43-1.45)
Target Range (n = 356)	1.18 (0.72-1.95)	0.50 (0.28-0.91)	0.57 (0.24-1.35)	0.51 (0.24-1.11)
Table 1: Odds ratios (OR) and 95% confidence intervals (CI) from multivariable logistic regression models for the association between vitamin D status with increased inflammatory biomarker concentrations (≥90 th percentile)

Whether the lower white blood cell counts above the target range are desirable may depend on whether you're suffering from an auto-immune disease. In general, they are yet another reason to keep the in mind that Mellenthin et al. are not the first to observe a non-linear, U-shaped dose-response relationship for the beneficial health effects of vitamin D.

There are exceptions to all "rules" - except from one: Testing makes sense, because low levels of 24OHD are far worse than high ones! Whether or not 25OHD levels way beyond the sufficiency range of 30ng/ml (75mmol/l) will promote or impair your health will depend on many factors. Autoimmune diseases, as mentioned before, may be one. In view of the fact that most 99% of the reported benefits were observed in subjects with insufficient, if not deficient pre- (at the beginning of the experiment) vitamin D levels, even these alleged benefits are in no way certain. I mean, look at the data in Figure 2 (right). Even in otherwise healthy people it's way better to have slightly high D levels than extremely low ones. In the end, the best way to make sure you are doing fine is to test: As long as you hover in the 28-40ng/ml range yearlong, there is nothing to freak out about.

In this case this was a reduction in overall inflammation. In previous studies similar U-shaped, non-linear dose-response relationships were observed for

• Did you know? Seasonal variation in serum 25(OH)D is between 10 and 20 nmol/L. Sunscreen use decreases, but does not abolish, vitamin D production in the skin. A high dietary calcium intake has a vitamin D-sparing effect, because it increases the half-life of 25(OH)D. A combination of sunlight exposure, nutrition, food fortification, and supplements is desirable to obtain sufficient vitamin D status in the population of most countries throughout the year (Lips. 2014).
  pre-hospital vitamin D status and mortality in a recent paper in the Journal of Clinical Endocrinology & Metabolism (Amerin. 2014),
• serum 25‐Hydroxyvitamin D and fracture risk in older men in the Prospective Population Based CHAMP Study (Bleicher. 2014),
• the maternal and newborn vitamin D status and its impact on food allergy development in the German LINA cohort study (Weisse. 2013)
• the population-wide cancer risk (White. 2013)
• the duration of hospital stays after cardiac surgery (Zittermann. 2013), 
• the association between vitamin D & mortality and morbidity based on data for 1 282 822 Clalit Health Services members aged >45 between July 2007 and December 2011 (Dror. 2013)

I could extent this list endlessly, but I honestly have better things to do, so let's stick to that and say: The notion that "more vitamin D" equals better health is obviously more than questionable. 

Figure 2: 25OHD levels and survival (left) and calculated risk for (right) of increased mortality in 1 282 822 Clalit Health Services members aged >45 between July 2007 and December 2011 (Dror. 2013)

Needless to say you are better off in the high 25OHD region (Figure 2, right >28-32), but if your goal is to avoid dying within the next 60 months, the previously cited study by Dror is only one of many references that would suggest that you are better of in the happy medium.

Studies like Close et al. (2013) leave little doubt that it does not take tons of vitamin D to get lowish levels back into the normal range - in fact, taking too much, in this case 40,000 IU per week, will take you into a 25OHD range, where the benefits are starting to diminish. Still, even here you're better off than you'd be with "officially low" 25OHD levels of <25ng/ml.

Bottom line: Vitamin D does not break the "more is not more"-rule of medical sciences. Instead of thriving to bring your vitamin D levels up into the hilarious D-council levels, you'd do yourself or rather your overall health a favor if you  hovered around in the normal zone.

This does not mean that you should try to avoid being deficient at all costs. So, how much do you need? Well, assuming that most of you are young(er) and active, you can follow the same protocol as the young healthy men in a 6-week trial by Close et al. whose previously low levels jumped up to >30 ng/ml was only 20 000 IU per week (for older subjects and/or subjects with (pre-)diabetes / other chronic disease with inflammatory component, twice the dosage may be necessary; cf.  Davidson. 2014).

A means to ensure sufficiency for the misers who are to cheap to test, would thus be taking 5,000IU every day for 1 month and a maintenance dose of 1,000IU/day or 10,000IU once per week to maintain optimal levels (Is it better to take your D and other fat soluble vitamins w/ fat? learn more) .

Reference:

• Amrein, Karin, et al. "Evidence for a U-shaped relationship between pre-hospital vitamin D status and mortality: a cohort study." The Journal of Clinical Endocrinology & Metabolism (2014).
• Bleicher, Kerrin, et al. "U‐Shaped Association Between Serum 25‐Hydroxyvitamin D and Fracture Risk in Older Men: Results from the Prospective Population Based CHAMP Study." Journal of Bone and Mineral Research (2014).
• Close, Graeme L., et al. "The effects of vitamin D3 supplementation on serum total 25 [OH] D concentration and physical performance: a randomised dose–response study." British journal of sports medicine 47.11 (2013): 692-696. 
• Davidson, Mayer B., et al. "High-dose vitamin D supplementation in people with prediabetes and hypovitaminosis D." Diabetes Care 36.2 (2013): 260-266.
• Dror, Yosef, et al. "Vitamin D levels for preventing acute coronary syndrome and mortality: evidence of a nonlinear association." The Journal of Clinical Endocrinology & Metabolism 98.5 (2013): 2160-2167.
• Mellenthin, Liesa, et al. "Association Between Serum Vitamin D Concentrations and Inflammatory Markers in the General Adult Population." Metabolism (2014).
• Lips P, van Schoor NM, de Jongh RT. "Diet, sun, and lifestyle as determinants of vitamin D status." Ann N Y Acad Sci. (2014).
• Weisse, K., et al. "Maternal and newborn vitamin D status and its impact on food allergy development in the German LINA cohort study." Allergy 68.2 (2013): 220-228.
• White, John H. "Vitamin D and human health: more than just bone." Nature Reviews Endocrinology 9.10 (2013): 623-623.
• Zittermann, Armin, et al. "Vitamin D status and the risk of major adverse cardiac and cerebrovascular events in cardiac surgery." European heart journal 34.18 (2013): 1358-1364.

There is More To Glucose Control Than Carbohydrates (3/?): Non-Carbohydrate Nutrients And Their Effects On Blood Glucose Management ➲ Vitamin D - The Sunshine Vitamin

Is the vitamin D you produce at the beach you're visiting only rarely the secret to perfect glucose control?

In the past two weeks you've learned much about the unquestionably beneficial effects of protein on glucose metabolism and the ambigous, since "context depend" effects of various fatty acids. Today, in the third installment of this series, we are leaving the "macros" behind and turning our heads towards the micronutrients.

I have long thought about the micros I would include in today's installment, started out with vitamin D and realized: "Damn! 50% of my Sunday gone already." In other words, you will have to live with the fact that today's installment of this series is an homage to the hype.

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Vitamin D unquestionably is a top candidate for the "micronutrient with the most bullshit science published", and contrary to what the mainstream media articles would suggest, it's by no means the panacea as which it is depicted even in "scientific" reviews, of which I am pretty sure that 90% of them are solely written to get published - I mean, every editor wants a vitamin D article in his journal, right?

Before this whole article turns into a rant, I'd suggest we take a look at the facts: It's beyond doubt that there are clear-cut (epidemiological determined) correlations between low vitamin D levels, insulin resistance and type II diabetes (Need. 2005). As a SuppVersity Reader you do yet know better than some of the previously mentioned scientists who will - without the blink of an eye - make the transition from "There is a correlation between low vitamin D levels and insulin resistance in our data" to statement like these:

• Vitamin D is an acute phase reactant - but what are the impli- cations? Firstly, this would imply that serum 25-hydroxy- vitamin D is an unreliable biomarker of vitamin D status after an acute inflammatory insult (for the obese, even a meal is an acute inflammatory result; Blackburn. 2006). Secondly, hypovitaminosis D may be the consequence rather than the widely purported cause of a myriad of chronic diseases (Gama. 2012).
  "Low vitamin D causes / triggers insulin resistance." -- An excellent example of someone confusing correlation and causation. What is often accepted as a scientific fact, is possible. In view of the fact that vitamin D has recently been shown to act as an acute phase reactant in inflammatory conditions, it is yet rather unlikely. In fact, it appears more likely that what we are seeing here is a correllative reduction of vitamin D, whenever someone - like a type II diabetic, for example - is chronically inflamed (Waldron. 2013)
• "Vitamin D supplements can be used to ameliorate insulin sensitivity." -- In an assertion like this, the authors go even one step further. After making the unwarranted conclusions that vitamin D triggers the onset of insulin resistance, they assume that supplemental vitamin D (usually D3), of which the current evidence shows that it does not elevate the levels of 1,25-hydroxy vitamin D, i.e. calcitriol, the only form of vitamin D, of which we actually have some rodent data that it's exogenous administration produces the anti-diabetic + weight loss effects everyone appears to expect from "regular" D3. An immediate effect of calcitriol on glucose uptake does yet not appear to exist - at least not in healthy individuals (Fliser. 1997).

When you're looking at the previously cited study by Filser, you could rightly argue that it is unrealistic too expect an already "optimal" insulin sensitivity to improve... and you are right! Studies like the one by Fliser et al. can thus hardly serve as a yardstick to gauge the usefulness of vitamin D

Figure 1: If we compare the fat "loss effects" of vitamin D supplementation in the studies by Zitterman (2009) and Salehpour (2012) in Figure 1 (left), and invoke the results of the latest meta-analysis by Pathak, et al. (2014) in Figure 1 (right), it is hard to argue Pathak's conclusion that the divergent results from previous trials would suggest that "Vitamin D supplementation did not decrease measures of adiposity in the absence of caloric restriction" (Pathak. 2014).

The studies we have to look for are studies with subjects who have a compromised glucose metabolism or full-blown type II diabetes (note: we cannot look at studies in type I diabetes, because any benefits vitamin D would provide here are most likely related effects on the immune system). Studies like these, for example:

• Inomata (1986) - 1-alpha (OH)D3 (active vitamin D) administration improves glucose tolerance in diabetic subjects
• Nilas (1983) - No effect of vitamin D or its analogues on body weight or glucose management in post-menopausal women
• Orwoll (1994) - No effect of calcitriol (active vitamin D) on glucose homeostasis in non-insulin-dependent diabetes mellitus

Figure 2: The latest meta-analysis says: No long-term improvement in blood glucose management w/ vitamin D supplements (George. 2012).

I could add one study after the other, but I know what you are thinking right now: Who cares about studies on vitamin D sufficient individuals?

You're right. If we don't make the totally irrational, yet not uncommon assumption that the initially mentioned correlation between low vitamin D and low insulin sensitivity would apply beyond deficiency levels. There is thus no reason to assume that supplementation would help anyone with normal vitamin D levels so that we have to focus on those individuals with an impaired insulin resistance who are actually vitamin D deficient.

"Our results suggest that hyperinsulinemia and/or insulin resistance are directly responsible for decrease of 25(OH)D levels in obesity." (Pergola. 2013) That's the logical conclusion from a closer analysis of the correlation between low vitamin D and insulin resistance that revealed that 25(OH)D levels are negatively associated with inflammatory parameters such as CRP and C3 and C4 levels, but not independently of BMI, body fat distribution, insulin levels, or insulin resistance.

Unfortunately (for the average vitamin D enthusiast), the situation is not entirely unambiguous in this population either. Even in studies on vitamin D deficient subjects, you will find quite impressive null results (impressive, because the D-levels increase significantly, but nothing happened), though. Tai et al., for example, found no improvements in insulin sensitivity in spite of the fact that the vitamin D supplement they had administered to their 33 vitamin D insufficient subjects (serum 25-hydroxyvitamin D concentration ≤50 nmol/L; 12 with impaired glucose tolerance) increased their 25OHD levels from 39.9 ± 1.5 (SEM) to 90.3 ± 4.3 nmol/L (Tai. 2008).

Rule of thumb: If anyone is actually likely to benefit, though, it's the overweight, inflamed (pre-)diabetic, for whom George et al. calculated a small effect on fasting glucose (−0.32 mmol/l) and a small improvement in insulin resistance (standard mean difference −0.25), but no improvements in long-term glucose management (HbA1c, see Figure 2) in response to vitamin D supplementation (George. 2012).

Figure 3: No improvement in insulin sensitivity in people w/ normal, min. effects in those with compromised insulin sensitivity w/ vitamin D supplements, says meta-analysis (George. 2012).

As with every "rule" there are exceptions to this one, as well. Nagpal et al. for example observed that the provision of three doses of vitamin D3 (120 000 IU each; supplemented group) improved the postprandial glucose excursions of the abdominally obese, but allegedly "apparently healthy" subjects (Nagpal. 2009). The results of a paper by Belenchia from 2013, on the other hand, violate the "no improvements in long-term glucose management rule". The scientists from the University of Missouri School of Medicine did after all find that adding 4,000IU/day of vitamin D to a standard life-style intervention lead to significant improvements in blood glucose management in their adolescent subjects with low baseline vitamin D levels (Belenchia. 2013).

For someone with an established (=tested) vitamin D deficiency, supplementation does therefore appear to be clearly indicated. As long as you stick to reasonable amounts (see Recommendation I, below) there is little to no risk of doing any harm (although I know from anecdotes that some people react with fatigue to relatively slow quantities of vitamin D).

Recommendation #1: Unless you are a sun-worshipper living in a country near the equator, you want to make sure to get ~1,000IU, if you are normal-weight and light-skinned, or 2,000IU, if you are overweight and/or dark-skinned (Gallagher. 2013; Ng. 2014), vitamin D per day from food or supplements.

Figure 4: Increase in vitamin D levels in response to supplementation w/ different amounts of vitamin D3 in caucasian (!) women according to BMI categories (Gallagher. 2013)

In that, it does not matter, if you get to those 7,000-10,000 IU per week by taking a single cap of a high dose vitamin D supplement once a week, or adding enough cod liver (oil), fatty fish, fortified dairy, oysters, or eggs (remember there is active vitamin D in eggs | learn more) to your diet. What is important, though is recommendation #2, which is:

Recommendation #2: Get a 25OHD test done today and start supplementing with 20,000IU per week for 3 months, if the test comes back low - that's the dosage that has brought the low D3 levels of 30 club-level athletes in Close et al. (2013) back to the official and certainly not unreasonable target of >50 nmol/L.

Needless to say that recommendation #3 would be to retest either after 3 months, in case you had low baseline levels and want to make sure your supplementation regimen brought them back up, or after 6 months, as part of a bi-annual checkup of all relevant health parameters, including the standard blood panel and HPTA function.

Why shall I make sure my level is normal, if low vitamin D does not cause insulin resistance? That's a warranted question and I have an comprehensive answer. If vitamin D acts as an acute phase reactant this may mean that it protects your body from further pro-inflam- matory assaults - it's making a martyr of itself, so to say. If you have almost no "vitamin D martys" to sacrifice, this will accelerate your progress from insulin resistance to diabetes (cf. Forouhi. 2008)

Bottom line: Things are, I am sorry to say that yet again, complicated. My personal assessment of the contemporarily available evidence is that the reduced vitamin D levels are correlatively and not causally linked to insulin resistance. We've known forever that chronic inflammation is a if not the most common cause of insulin resistance (Johnson. 2013) and vitamin D, whether it is an acute phase reactant or the panaceum everyone is trying to tell you it was, is reduced under inflammatory conditions.

In view of the fact that the provision of additional vitamin D and restoration of "normal" (whatever that may be) levels of 25OHD3 in serum does not necessarily entail an improvement in insulin sensitivity, we must therefore assume that both, low vitamin D and insulin resistance have the same underlying cause and are thus complementary. Dies this mean, you should ignore low vitamin D levels? Probably not, but it certainly means that you better take a look at the way you eat, sleep and train if you are insulin resistant - irrespective of your vitamin D levels, by the way.

References:

• Belenchia, Anthony M., et al. "Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomized controlled trial." The American journal of clinical nutrition 97.4 (2013): 774-781.
• Blackburn, Patricia, et al. "Postprandial variations of plasma inflammatory markers in abdominally obese men." Obesity 14.10 (2006): 1747-1754. 
• Close, Graeme L., et al. "The effects of vitamin D3 supplementation on serum total 25 [OH] D concentration and physical performance: a randomised dose–response study." British journal of sports medicine 47.11 (2013): 692-696.
• Fliser, D., et al. "No effect of calcitriol on insulin‐mediated glucose uptake in healthy subjects." European journal of clinical investigation 27.7 (1997): 629-633.  
• Forouhi, Nita G., et al. "Baseline serum 25-hydroxy vitamin d is predictive of future glycemic status and insulin resistance the medical research council ely prospective study 1990–2000." Diabetes 57.10 (2008): 2619-2625.
• Gama, Rousseau, et al. "Hypovitaminosis D and disease: consequence rather than cause." BMJ 345 (2012): e5706-e5706.
• Gallagher, J. Christopher, Vinod Yalamanchili, and Lynette M. Smith. "The effect of vitamin D supplementation on serum 25OHD in thin and obese women." The Journal of steroid biochemistry and molecular biology 136 (2013): 195-200. 
• George, P. S., E. R. Pearson, and M. D. Witham. "Effect of vitamin D supplementation on glycaemic control and insulin resistance: a systematic review and meta‐analysis." Diabetic Medicine 29.8 (2012): e142-e150. 
• Johnson, Andrew MF, and Jerrold M. Olefsky. "The origins and drivers of insulin resistance." Cell 152.4 (2013): 673-684.
• Inomata, S., et al. "Effect of 1 alpha (OH)-vitamin D3 on insulin secretion in diabetes mellitus." Bone and mineral 1.3 (1986): 187-192. 
• Nagpal, J., J. N. Pande, and A. Bhartia. "A double‐blind, randomized, placebo‐controlled trial of the short‐term effect of vitamin D3 supplementation on insulin sensitivity in apparently healthy, middle‐aged, centrally obese men." Diabetic Medicine 26.1 (2009): 19-27.
• Need, Allan G., et al. "Relationship between fasting serum glucose, age, body mass index and serum 25 hydroxyvitamin D in postmenopausal women." Clinical endocrinology 62.6 (2005): 738-741.
• Ng, Kimmie, et al. "Dose response to vitamin D supplementation in African Americans: results of a 4-arm, randomized, placebo-controlled trial." The American journal of clinical nutrition (2014): ajcn-067777.
• Nilas, L., and C. Christiansen. "Treatment with vitamin D or its analogues does not change body weight or blood glucose level in postmenopausal women." International journal of obesity 8.5 (1983): 407-411.
• Orwoll, Eric, Matthew Riddle, and Melvin Prince. "Effects of vitamin D on insulin and glucagon secretion in non-insulin-dependent diabetes mellitus." The American journal of clinical nutrition 59.5 (1994): 1083-1087.
• Pathak, K., et al. "Vitamin D supplementation and body weight status: a systematic review and meta‐analysis of randomized controlled trials." Obesity Reviews (2014).
• Salehpour, Amin, et al. "A 12-week double-blind randomized clinical trial of vitamin D3 supplementation on body fat mass in healthy overweight and obese women." Nutr J 11.1 (2012): 78.
• Tai, Kamilia, et al. "Glucose tolerance and vitamin D: effects of treating vitamin D deficiency." Nutrition 24.10 (2008): 950-956.
• Waldron, Jenna Louise, et al. "Vitamin D: a negative acute phase reactant." Journal of clinical pathology 66.7 (2013): 620-622.
• Zittermann, Armin, et al. "Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers." The American journal of clinical nutrition 89.5 (2009): 1321-1327.